Proliferative signaling and disease progression in heart failure

Circulation Journal : Official Journal of the Japanese Circulation Society
Arnold M Katz

Abstract

Therapy for heart failure has traditionally been directed to such short-term functional abnormalities as low cardiac output, high filling pressures, and fluid retention. More recently, it has become clear that therapy must also inhibit the proliferative responses that contribute to the progressive deterioration of the failing heart. That heart failure is more than a hemodynamic disorder became apparent when clinical trials showed that drugs that improve such functional abnormalities as high venous pressure and low cardiac output failed to improve long-term prognosis. Most vasodilators, in spite of alleviating short-term problems caused by excessive afterload, increase long-term mortality; the notable exceptions are ACE inhibitors, the ability of which to prolong survival and inhibit remodeling can be attributed to inhibition of proliferative signaling. Other clinical trials showed that inotropic drugs, while providing immediate relief of symptoms, generally shorten long-term survival, whereas beta-adrenergic receptor blockers, which inhibit proliferative signaling by norepinephrine, improve prognosis. These findings can be explained by crossovers between functional and proliferative signaling, among the most important of which ...Continue Reading

References

Jul 1, 1975·The Journal of Clinical Investigation·W GrossmanL P McLaurin
Dec 4, 1975·The New England Journal of Medicine·A M Katz
Jan 11, 1990·The New England Journal of Medicine·A M Katz
Jul 14, 1988·The New England Journal of Medicine·M A PfefferE Braunwald
Jul 1, 1985·Circulation Research·J M PfefferE Braunwald
Sep 1, 1984·Annals of Internal Medicine·G S FrancisJ N Cohn
Jun 1, 1983·Cardiovascular Research·P Harris
Aug 31, 1995·Nature·H R Bourne
May 15, 1996·JAMA : the Journal of the American Medical Association·R E SchmiederA Klingbeil
Jun 15, 1996·Journal of Cellular Biochemistry·H AberleR Kemler
Feb 20, 1997·The New England Journal of Medicine·UNKNOWN Digitalis Investigation Group
Oct 23, 1997·Current Opinion in Cell Biology·F G Giancotti
Jan 1, 1997·Annual Review of Cell and Developmental Biology·A S YapB M Gumbiner
Feb 7, 1998·Hypertension·W A HsuehY S Do
Sep 10, 1999·The American Journal of Cardiology·M Packer, A B Miller
Sep 18, 1999·Cell·K R Chien
Nov 18, 2000·Circulation·A M Katz, B H Lorell
Aug 30, 2001·American Heart Journal·G M Felker, C M O'Connor

❮ Previous
Next ❯

Citations

Aug 2, 2003·Circulation Journal : Official Journal of the Japanese Circulation Society·Shinji SatohNaoki Makino
Mar 3, 2004·Circulation Journal : Official Journal of the Japanese Circulation Society·Satomi-Kobayashi SeimiYokoyama Mitsuhiro
Feb 2, 2016·Journal of Molecular and Cellular Cardiology·Toru OkaIssei Komuro
Nov 15, 2012·Medical Hypotheses·Yanmin XuYuzhi Liu
Jun 12, 2012·Heart, Lung & Circulation·Timothy C TanA Robert Denniss
Jan 17, 2012·The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation·Jeremias WohlschlaegerHideo Andreas Baba
Sep 21, 2010·The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation·Jeremias WohlschlaegerHideo Andreas Baba
Aug 21, 2010·Peptides·Gregory S HarrisChristopher J Wingard
Aug 28, 2013·International Journal of Cardiology·Zhiqiang ZhaoGuangping Li
Aug 29, 2006·Anais Da Academia Brasileira De Ciências·Patricia C BrumAlessandra Medeiros
Dec 20, 2011·Cardiology·Deepak SharmaYanmin Xu
Apr 1, 2008·Circulation. Arrhythmia and Electrophysiology·Stanley NattelDobromir Dobrev
Nov 27, 2007·Circulation Journal : Official Journal of the Japanese Circulation Society·Megumi KunishigeTakeshi Hata

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

Atopic Dermatitis

Atopic dermatitis is a chronic inflammatory genetically determined disease of the skin marked by increased ability to form reagin (IgE), with increased susceptibility to allergic rhinitis and asthma, and hereditary disposition to a lowered threshold for pruritus. Discover the latest research on atopic dermatitis here.

Adrenergic Receptors: Trafficking

Adrenergic receptor trafficking is an active physiological process where adrenergic receptors are relocated from one region of the cell to another or from one type of cell to another. Discover the latest research on adrenergic receptor trafficking here.

Cardiac Remodeling

Cardiac remodeling in response to a myocardial infarction is characterized by progressive ventricular dilatation, cardiac hypertrophy, fibrosis, and deterioration of cardiac performance. Discover the latest research on Cardiac Remodeling here.

Adhesion Molecules in Health and Disease

Cell adhesion molecules are a subset of cell adhesion proteins located on the cell surface involved in binding with other cells or with the extracellular matrix in the process called cell adhesion. In essence, cell adhesion molecules help cells stick to each other and to their surroundings. Cell adhesion is a crucial component in maintaining tissue structure and function. Discover the latest research on adhesion molecule and their role in health and disease here.

Arrhythmogenic Right Ventricular Dysplasia

Arrhythmogenic right ventricular dysplasia is a congenital cardiomyopathy that is characterized by infiltration of adipose and fibrous tissue into the right ventricle wall and loss of myocardial cells. Primary injuries usually are at the free wall of the right ventricular and right atria resulting in ventricular and supraventricular arrhythmias. Discover the latest research on arrhythmogenic right ventricular dysplasia here.